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Cyclin-Dependent Kinase 9 Proteins (CDK9)

On www.antibodies-online.com are 10 Cyclin-Dependent Kinase 9 (CDK9) Proteins from 5 different suppliers available. Additionally we are shipping CDK9 Antibodies (144) and CDK9 Kits (19) and many more products for this protein. A total of 179 CDK9 products are currently listed.

Human Cyclin-Dependent Kinase 9 (CDK9) interaction partners

H1 variant interphase phosphorylation is dynamically regulated in a site-specific and gene-specific fashion during pluripotent cell differentiation, and that enrichment of pS187-H1.4 at genes is positively related to their transcription. H1.4-S187 is likely to be a direct target of CDK9 during interphase, suggesting the possibility that this particular phosphorylation may contribute the release of pausedRNA pol II

CDK9 is a player in the DNA damage response and is consistent with its participation in homology-directed recombination pathway by modulating BRCA1 response.

Quantitative measurement of the molecular interactions among Tat (show TAT Proteins), CycT1 (show CCNT1 Proteins) and CDK9 has showed that any third molecule enhances the binding between the other two molecules. These findings suggest that each component of the Tat:P-TEFb (show TEF Proteins) complex stabilizes the overall complex, thereby supporting the efficient transcriptional elongation during viral RNA synthesis.

We could conclude that there are many small molecules that bind to CDK9, but their lack of selectivity against other CDKs do not allow them to get to the clinical use

Findings indicate that cyclin-dependent kinase 9 (CDK9) represent an important role for inflammation in the pathogenesis of atherosclerosis.

Studies indicate that CDK9 regulates the genetic transcription at the early-elongation checkpoint close to poly(A) sites just before a functional polyadenylated mRNA is produced.

Our findings suggest a potential role of CDK9 in the radiation response of head and neck squamous cell carcinoma cells

Data show that the CDK9 and cyclin T1 (show CCNT1 Proteins) subunits of P-TEFb (show CCNT1 Proteins) are present in mouse oocytes and preimplantation embryos, and that CDK9 is essential for embryonic genome activation in the mouse.

The present study examined whether Cdk9 forms a complex with GATA4 (show GATA4 Proteins) in mouse embryonic stem cells and is involved in their differentiation into cardiomyocytes.

Data report that a second cdk9 isoform, termed cdk9-55, plays a fundamental role in muscle regeneration and differentiation in vivo.

CDK9 has the intrinsic property to shuttle between nucleus and cytoplasm, and enhanced expression of cyclin T1 (show CCNT1 Proteins) promotes its nuclear localization.

chronic activation of Cdk9 causes not only cardiomyocyte enlargement but also defective mitochondrial function, via diminished PGC-1 transcription, and a resulting susceptibility to apoptotic cardiomyopathy

Zebrafish Cyclin-Dependent Kinase 9 (CDK9) interaction partners

CDK9 clearly plays a fundamental role in early cellular growth and proliferation.

Pharmacological and genetic results present evidence that CDK9 is involved in the resolution of neutrophil-dependent inflammation.

The balance of Cdk9 and Larp7 (show LARP7 Proteins) plays a key role in cardiomyocyte proliferation and response to injury

CDK9 Protein Profile

Protein Summary

The protein encoded by this gene is a member of the cyclin-dependent protein kinase (CDK) family. CDK family members are highly similar to the gene products of S. cerevisiae cdc28, and S. pombe cdc2, and known as important cell cycle regulators. This kinase was found to be a component of the multiprotein complex TAK/P-TEFb, which is an elongation factor for RNA polymerase II-directed transcription and functions by phosphorylating the C-terminal domain of the largest subunit of RNA polymerase II. This protein forms a complex with and is regulated by its regulatory subunit cyclin T or cyclin K. HIV-1 Tat protein was found to interact with this protein and cyclin T, which suggested a possible involvement of this protein in AIDS.